Medical Microbiology made memorable - part 5 pptx

M E D I C A L MICROBIOLOGY 52 Hepatitis and pancreatitis I nfection of the liver and pancreas occurs via the blood stream, rarely from the gastrointestinal tract, even when the route of acquisition is faecal-oral. Biliary tract infection and peritonitis are, conversely, due to locally spread infection. Hepatitis The classic clinical triad of jaundice, dark urine and pale stools accompanying fever is often missing, particularly in children, who are more often asymptomatic. The vast majority of cases are of viral aetiology, with hepatitis A, B and C being the commonest ( Table 22.1). Diagnosis of viral (and leptospiral) infection is serological, by either detection of antigen or specific antibody. The detection of hepatitis B surface antigen ( HBsAg) confirms the diagnosis of hepatitis B virus, and the presence of hepatitis B 'e' antigen ( HBeAg) indicates a high infectious risk. Other markers are determined in specific cases (Fig. 22.1). Jaundice in carriers, in whom HBsAg persists for 6 months or more, is most likely to have another cause, which should be sought. Hepatitis A virus ( HAV) infection is diagnosed by anti-HAV 1gM. Serological assays for the diagnosis of hepatitis C do not offer early diagnosis, as they are based on the detection of specific IgG, which may take several weeks; diagnosis is thus retrospective but can be made early by gene amplification methods such as PCR. Management of acute viral hepatitis is supportive, with bed rest at the peak of liver inflammation. Chronic hepatitis therapy is evolving, with drugs such as interferon, immunomodulators and ribavirin being used with moderate success in delaying progression of liver disease, although viral eradication is not achieved. Prevention of infection involves public health measures and vaccination for hepatitis A and hepatitis B. Travellers from the UK to higher-prevalence areas (outside northern and western Europe and North America) should consider vaccination for hepatitis A. Although universal vaccination for hepatitis B is being introduced in several countries, in the UK it is targeted at higher-risk groups, such as medical, nursing and laboratory staff, 'gay' men, and residents of mental institutions. In the event of contacts with both hepatitis A and hepatitis B, passive immunisation is available for susceptible individuals. About 10% of cases of hepatitis do not have an identifiable cause, and new viruses such as hepatitis G and TT virus have been discovered by modern molecular methods in some cases. Their aetiological role has, however, yet to be defined. Liver abscess These may be primary infections or secondary to haematogenous spread from another site. Usually bacterial, with mixed anaerobic and aerobic flora (including Enterobacteriaceae and Streptococcus milleri group), they consist of pus that has been walled off by a fibrinous layer; this can be detected by i maging. Single lesions are often asymptomatic unless very large. Broad-spectrum antibiotics are used to treat the condition, but surgical drainage may also be required. Biliary tract infection This occurs secondary to obstruction - either gallstones or malignancy. Ascending cholangitis, liver abscess and septicaemia may be sequelae. Diagnosis is clinical, with imaging used as a confirmatory test. Treatment consists of removal of the obstruction and broad-spectrum antibiotics. Peritonitis Contamination of the sterile peritoneal cavity occurs through breach of the bowel or urogenital wall. This may be iatrogenic, such as occurs in surgery, or through diseases such as inflammatory bowel disease, appendicitis and malignancy. Occasionally tuberculosis or actinomycosis of the genital tract may have been the initial site of infection. Genital chlamydia and gonococcal infections can also ascend to cause perihepatitis (so-called FitzHugh-Curtis syndrome). Clinical diagnosis is confirmed operatively, or through laparoscopy, with pus and/or adhesions visible between the peritoneal layers. Treatment with broad-spectrum antibiotics may be required, as infections arising from the gut are polymicrobial. Panereatitis This can be caused by a number of viruses (Table 22.2). Mumps is the commonest. Diabetes mellitus is associated with preceding enterovirus infection. Bacteria can cause pancreatitis, with mixed flora, if there is obstruction at the ampulla of Vater, usually due to malignancy. FIG 22.1 Time course of markers in hepatitis B infection I nfective causes of acute pancreatitis Mumps Enteroviruses Cytomegalovirus Epstein-Barr virus Mixed bacterial flora 5 3 I nfective causes of hepatitis Cause Route of transmission Characteristic features Hepatitis A Faecal-oral I ncubation period of 2-4 weeks. <11% of cases Hepatitis B Blood-borne are fulminant I ncubation period of 1-3 months. Immune complex Hepatitis C Blood-borne form and may cause arthralgia, urticarial rash and glomerulonephritis. 10% become chronic carriers, with subsequent chronic hepatitis, cirrhosis and hepatocellular carcinoma. High prevalence of i nfection, carriage and hepatoma in S.E. Asia I ncubation period of 2-4 months. 90% become Hepatitis D Blood-borne carriers Defective virus requiring hepatitis B or herpes Hepatitis E Faecal-oral simplex to replicate. Co-infection with hepatitis B makes it more severe; super-infection results in recurrence I ncubation period 6-8 weeks. Water-borne Leptospira interrogans Faecal-oral epidemics have been seen in India and the former Soviet Union, with 20% mortality in pregnant women in 3rd trimester due to disseminated i ntravascular coagulation Spirochaetes can also enter through skin. (leptospirosis, Weils' disease) Sewerage workers at risk from infected rat urine. Enfamoeba histolytica May be complicated by aseptic meningitis and haemorrhages. Treatment i s with penicillin Causes pseudoabscess (amoebiasis) Parasitic infections Faecal-oral I nfections of mainly tropical climates (schistosomiasis, clonorchiasis, fascioliasis) Others (CMV, EBV, HSV, Various Usually part of generalised i nfection rubella, yellow fever, TB, toxoplasmosis, syphilis, etc.) M E D I C A L MICROBIOLOGY 54 I nfections of the heart Endocarditis is an uncommon but serious disease involving the endothelial lining of the heart, particularly the cardiac valves. Even with appropriate therapy there is a mortality rate of up to 30% - untreated mortality approaches 100%. In many patients, predisposing factors are found such as: •  congenital heart disease •  rheumatic heart disease •  degenerative heart disease •  other cardiac lesions, e.g. mitral valve prolapse •  i. v. drug usage •  prosthetic heart valve. Native valve endocarditis is distinguished from prosthetic valve endocarditis, which can be divided into early (occurring within 2 months of surgery) or late onset. The majority of cases of endocarditis are caused by bacteria, although fungi and other organisms are sometimes implicated ( Table 23.1). Organisms reach the valves following bacteraemia which may arise from a number of sources including dental procedures (e.g. extractions, scaling or even vigorous brushing), invasive instrumentation (e.g. bronchoscopy) or surgery of the gastrointestinal or genitourinary tracts. Adherence of organisms is enhanced by the presence of fibrin-platelet deposits on damaged endothelium and by bacterial factors such as adhesins and fibronectin-binding proteins. The accumulation of fibrin, platelets and organisms forms vegetations that may interfere with valvular function or form emboli to distant organs. The onset of endocarditis may be insidious and the diagnosis difficult, but the following clinical features may suggest the diagnosis: •  fever (often low-grade) •  general malaise with anorexia and weight loss •  new or changing heart murmurs •  embolic phenomena (especially skin and brain) •  i mmune complex disease (nephritis and some skin lesions, e.g. splinter haemorrhages). I nvestigations The haemoglobin may be reduced and white cell count and markers of an acute phase response such as plasma viscosity and C-reactive protein increased. Haematuria and proteinuria should be sought to indicate nephritis. Vegetations may be detected at transthoracic echocardiography, although transoesophageal examinations are more sensitive, particularly in prosthetic valve disease (Fig. 23.1). An essential element of diagnosis is blood culture, which should be undertaken before starting antimicrobial therapy. Three cultures should be taken from separate venepunctures at different times within 24 h. Scrupulous aseptic technique is essential, as skin organisms are generally contaminants but are also common pathogens in prosthetic valve endocarditis. Culture-negative endocarditis may be due to prior antimicrobial treatment or fastidious organisms that require special culture techniques or serology for their detection. Surgical material (valves, vegetations, pus, etc.) should be examined carefully by microscopy and culture. Management The importance of obtaining an isolate is that detailed susceptibility studies are i mportant in optimising antimicrobial treatment. The minimum inhibitory concentration (MIC) of antibacterials should be determined to ensure appropriate doses and duration of therapy. In most cases combination therapy is employed to provide enhanced activity: e.g. the addition of gentamicin to benzylpenicillin improves bactericidal activity against many streptococci and enterococci. High-dose regimens for several weeks are required for successful therapy, and clinicians should liaise closely with microbiologists to select and monitor therapy. Antibiotic levels (e.g. gentamicin, vancomycin) need monitoring closely, and serial measurements of C-reactive protein (together with temperature, white cell count and plasma viscosity) are helpful in assessing response. Where extensive valvular damage has occurred (and in most cases of prosthetic disease), valve replacement may be required in addition to antimicrobial therapy. Prophylaxis As bacteraemia may result in endocarditis in susceptible patients, prophylactic regimens are recommended for •  dental procedures •  genitourinary surgery or instrumentation •  gastrointestinal procedures •  obstetric and gynaecological procedures. These regimens are based on consensus statements and experimental evidence, as the incidence of endocarditis is too low to conduct controlled trials. Current detailed advice is given in the British National Formulary. Myocarditis and pericarditis Infection of the heart muscle or pericardium is often viral in origin, although pericarditis may present as a severe bacterial infection (Table 23.2). Typical symptoms include a 'flu'-like illness and localised pain. Myocarditis may cause dysrhythmia and, in severe cases, heart failure. In pericarditis a pericardial rub may be heard, and in severe cases, typically caused by pyogenic bacteria, effusion may be demonstrated by chest X-ray or echocardiography. Respiratory swabs and stool samples should be cultured for viruses, and blood and pericardial fluid (where available) cultured for bacteria. Viral infections are usually self-limiting, but bacterial infections require prompt treatment. Pathogens in myocarditis and pericarditis 5 5 Myocarditis Pericarditis Viruses Enteroviruses, especially coxsackie Enteroviruses, especially coxsackie Echovirus I nfluenza A & B I nfluenza A & B Rubella Epstein-Barr virus Cytomegalovirus Bacteria Coxiella burnetii Mycoplasma pneumoniae Leptospira spp. Strep. pneumoniae Mycoplasma pneumoniae Strep. pyogenes N. meningitidis Staph. aureus Mycobacterium tuberculosis Coxiella burnetii FIG 23.1 Aortic vegetation seen on echocardiography M E D I C A L MICROBIOLOGY 56 Urinary tract infections Urinary tract infections are more common at certain ages in males and females (Fig. 24.1). Whilst many infections are mild, renal infections may lead to long-term renal damage, and the urinary tract is a common source of life-threatening Gram-negative bacteraemia. Several clinical syndromes are recognised (Table 24.1), the commonest being lower urinary tract infection of the bladder (cystitis). Upper urinary tract i nfection (pyelonephritis) may result from haematogenous or ascending routes of infection. Pathogenesis The pathogenesis of urinary tract infections is summarised in (Table 24.2). The additional risk factors (including instrumentation and catheterisation) in hospitalised patients lead to a difference in the organisms isolated (Fig. 24.2). The normal urinary tract is sterile, but urine may be contaminated with organisms from the distal urethra during voiding. Kass defined the term significant bacteriuria as >10' colony-forming units (cfu) of a single organism per millilitre of urine. This figure was derived from studies in women and was found to distinguish pyelonephritis from contamination. However, despite regular usage since, this figure is not validated for other urinary infections or those in men or children. In patients with symptomatic infections, counts may be as low as 10 2 cfu/ml. About 50% of women who present with the clinical features of cystitis do not have positive urine cultures, a condition known as abacterial cystitis or 'urethral syndrome'. The aetiology of this condition is controversial, but explanations include: •  i nfection with low counts of bacteria •  infection with fastidious organisms not detected on routine culture •  sexually transmitted infections, e.g. chlamydia •  non-infective inflammation, e.g. chemical. Asymptomatic bacteriuria occurs in about 5% of women and is important in pregnancy, where, untreated, 20-30% of cases will develop acute pyelonephritis. Bacteriuria in pregnancy is also associated with premature birth, low birth weight and increased perinatal mortality. It is therefore i mportant that all women have their urine cultured early in pregnancy. Microbiological investigations and interpretation Urine specimens need to be collected with care to minimise contamination with periurethral organisms. The first portion of voided urine is discarded and a midstream urine ( MSU) specimen collected. Specimens from catheterised patients should be collected by needle aspiration from the catheter tubing. In children specimens may be collected in adhesive bags, but, to avoid contamination, suprapubic aspiration may be required. Where there may be a delay in examination, specimens should be refrigerated or collected in containers with boric acid to prevent bacterial multiplication in transit. Microscopy for white and red blood cells may be helpful in the interpretation of culture results, but their presence does not necessarily indicate urinary tract infection. Squamous epithelial cells usually indicate contamination of the specimen. Quantitative culture is followed by susceptibility testing of significant isolates. Some clinicians and laboratories use screening methods to exclude urinary infection. Dipstick tests are available for the detection of blood, leucocyte esterase (indicating white blood cells) and nitrite (indicating the presence of nitrate-reducing bacteria). The interpretation of culture results depends on clinical details (symptoms, previous antibiotics), quality of specimen, delay in culture and species isolated. Repeat specimens may be required with low bacterial counts, evidence of contamination or so-called 'sterile pyuria' - white blood cells i n the urine without bacterial growth. This may be caused by: •  prior antibiotics •  urethritis (chlamydia or gonococci) •  vaginal infection or inflammation •  fastidious organisms (controversial significance) •  non-infective inflammation (e.g. tumours, chemicals) •  urinary tuberculosis. Where tuberculosis is considered, three early morning urine specimens should be collected for culture when the urine is most concentrated. Treatment Uncomplicated cystitis should be treated with a short (typically 3 day) course of an oral antibacterial agent such as trimethoprim or nitrofurantoin. Post-treatment follow-up cultures are particularly important in children and pregnant women. For patients with complicated infections, antibiotics such as cephalosporins or gentamicin are often indicated depending on antibiotic susceptibility (Fig. 24.3). In catheterised patients, antimicrobial treatment is usually only recommended in patients with systemic features. The catheter should be removed whenever possible. Pyelonephritis requires treatment, initially systemic, for a total of 10-14 days. In selected cases a prophylactic dose of an antibacterial agent given at night may reduce the incidence of recurrent cystitis. FIG 24.3 Susceptibilities of (a) hospital urine isolates to tri methoprim (b) GP urine isolates to trimethoprim 5 7 Clinical syndromes of the urinary tract Lower urinary tract Bacterial cystitis Frequency and dysuria, often with pyuria and Abacterial cystitis haematuria As above but without significant bacteriuria' Prostatitis Fever, dysuria, frequency with perinea) and Upper urinary tract Acute pyelonephritis l ow back pain Symptoms of cystitis plus fever and loin pain chronic interstitial Renal impairment following chronic inflammation nephritis - i nfection one of many causes Asymptomatic covert bacteriuria Detected only by culture. I mportant in children and pregnancy Pathogenesis of urinary tract infections Host factors Shorter urethra Obstruction Neurological problems Ureteric reflux More infections in females Enlarged prostate, pregnancy, stones, tumours I ncomplete emptying, residual urine Ascending infection from bladder, especially in children Bacterial factors Faecal flora Potential urinary pathogens colonise Adhesion periurethral area Fimbriae and adhesins allow attachment to K antigens urethra) and bladder epithelium Allow some E. toll to resist host defences by Haemolysins producing polysaccharide capsule Damage membranes and cause renal damage Urease Produced by some bacteria, e.g. Proteus FIG 24.1 Prevalence of urinary tract infections by age FIG 24.2 Urine isolates in hospital and general practice 58 M E D I C A L MICROBIOLOGY Genital tract infections This category includes a number of sexually transmitted diseases (STDs) that affect the genital tract, as well as some infections that do not require sexual activity for transmission (Fig. 25.1). Sexually transmissible infections whose main symptoms occur outside the genital tract, e.g. HIV and Hepatitis B, are considered elsewhere. STDs require intimate contact for transmission, the rates generally being highest from male to female. The site of infection will depend upon the nature of the sexual act that was performed. Contact tracing is undertaken following diagnosis of an STD to reduce transmission within the community, and, for this reason, general practitioners will often refer patients to the local genitourinary clinic where all the facilities are available. Having declined in recent years, probably because of individuals' precautions against HIV infection, the rates of all STDs now appear to be rising again. The laboratory methods of diagnosis and the treatments for genital infections are summarised in Table 25.1. In the male, with the exception of the distal 2-3 cm, the normal urethra is sterile, protected by mucus, prostatic secretions and periodic flushing with urine. The commensal flora of the vagina offers some protective effect in the female, as does the mucus within the cervix and the uterine cell turnover through menstruation. Skin infections (both sexes) Herpes simplex is a relapsing condition that produces multiple painful ulcers on the genital skin and mucous membranes following a variable prodrome of tingling. Human papilloma virus infection is generally a self-limiting condition marked by non-painful warts or dry scaling lesions on the genital skin; although it is less obvious, mucosal surfaces may also be infected with certain types of virus, bringing an increased risk of carcinoma, particularly of the cervix. Syphilis is a multisystem disorder diagnosed serologically and caused by the bacterial spirochaete Treponema pallidum. The disease is now rare. More common in the tropics are three ulcerative conditions with regional lymphadenopathy - chancroid, granuloma inguinale, lymphogranuloma venereum - caused by H. ducreyi, Calymmatobacterium granulomatis, and Chlamydia trachomatis serotypes L1-L3, respectively. I nfection in the male Urethritis in males is usually symptomatic, with discharge and dysuria. C. trachomatis serotypes D-K are the most common cause, although more severe symptoms suggests infection with N. gonorrhoeae. Mixed infections are common. Urethritis may progress to involve the prostate or epididymis, which may be more difficult to treat. Reiter's syndrome (urethritis, iritis and arthritis) is an unpleasant relapsing condition that may follow an episode of urethritis, particularly in HLA B27 carriers. Proctitis is most common amongst male homosexuals, with rectal pain, bleeding and discharge. Apart from the known causes listed in Fig. 25.1, other changes in bowel flora occur (e.g. the acquisition of novel Cam pylobacter species) the significance of which is unclear. I nfection in the female Silent infections are common in women. N. gonorrhoeae may cause infection of Bartholiri s glands at the vaginal introitus, although other bacteria can also be responsible. Vaginal discharge is a common reason for medical consultation, and an accurate diagnosis may usually be obtained in the surgery from a vaginal swab using the features described in Table 25.2. Candidiasis is a very common problem that is more likely with the contraceptive pill, pregnancy, diabetes and following the use of antibiotics. Similarly, anaerobic or bacterial vaginosis is caused by a disturbance in the normal vaginal flora, often following the use of broad-spectrum antibiotics. If the problem is seen to arise from the cervical os and not the vagina, samples of the discharge should be sent to the microbiology laboratory for more-detailed analysis. The causes of cervical infection are all sexually transmitted, with chlamydia being the most common. Whilst infection may often be a symptomatic, it is still a reservoir for spread to others through sexual contact and for ascending infection. Pelvic inflammatory disease (PID) may present as an acute peritonitis, as chronic pelvic pain and dyspareunia or be clinically silent. Regardless of the presentation, there is a significant risk of damage to the Fallopian tubes, leading to an increased incidence of ectopic pregnancy and infertility. Treatment will often involve the 'blind' use of antibiotics, as a microbiological diagnosis is unlikely unless laparoscopy is performed. 5 9 Detection and treatment of genital tract infection I nfectious agent Method of detection Treatment of choice Herpes simplex virus Human papilloma virusa Clinical, viral culture, electron microscopy Clinical only Aciclovir or related drug Chemical or surgical removal N. gonorrhoeae C. trachomatis Mycoplasma genital/urn T pallidum Anaerobic vaginosis ( Gardnerella vaginalis anaerobes) Haemophilus ducreyi Calymmatobacterium granuloma fix Culture, microscopy, DNA amplification Antigen detection, DNA amplification, (tissue culture) Culture Antibody detection Culture, microscopy Microscopy & culture Culture Ciprofloxacin, 3rd generation cephalosporin, azithromycin Tetracycline, azithromycin Tetracycline Penicillin Metronidazole, (co-amoxyclav) Erythromycin Tetracycline Candida spp. Microscopy, culture Fluconazole, (nystatin) Trichomonas vaginalis Microscopy, culture Metronidazole ASexually transmitted diseases Discharge from the female genital tract I nfection/condition Site pH KOH Microscopy clinical features Normal Vagina <4.5 - Lactobacilli Minimal discharge, variable colour Candidiasis Vagina <4.5 - Budding yeasts/hyphae Yellowish-white discharge/plaques, pruritus Trichomoniasis Vagina > 4.5 Malodour Motile parasites Profuse frothy foul-smelling yellow-green discharge, Bacterial vaginosis Vagina > 4.5 Malodour Clue cells vaginal petechiae Foul-smelling grey-white discharge, pruritus, dyspareunia +++ Gram-negative bacilli Gonorrhoea C. trachomatis i nfection Cervix Cervix Unhelpful Unhelpful Asymptomatic -u moderate mucopurulent discharge Asymptomatic -u moderate mucopurulent discharge FIG 25.1 Anatomy of sexually transmitted disease M E D I C A L MICROBIOLOGY 62 Obstetric and neonatal infections Both the pregnant woman and the newborn infant are to some extent immunocompromised. Most infections in pregnancy are not more common (an exception is urinary tract infection) but are more likely to be severe or reactivate (Table 26.1). Primary infection in the mother induces IgM antibodies, but these do not pass the placenta to the fetus. Infection may result in fetal death and spontaneous abortion or congenital infection and associated malformations. The baby may also acquire infection around the ti me of birth (perinatal infection) or after birth (postnatal infection). Infections diagnosed in the first 3 months after birth are termed neonatal infections. Prenatal / congenital infections Most congenital infections (Table 26.2) follow primary maternal infection, but reactivation of CMV in pregnancy can lead to infection of the fetus. Many of the organisms responsible for congenital infections may also cause spontaneous abortion. Typically, most foetal infections are associated with mild or subclinical infections in the mother. Diagnosis depends on clinical suspicion, contact history enhanced by serology of maternal blood. Confirmation may be made, via cordocentesis, by serology or PCR of fetal blood. First-trimester primary rubella infection caries such a high risk to the fetus of subsequent congenital rubella syndrome, that termination is usually advised if spontaneous abortion does not occur. Rubella infection after the fourth month does not pose a significant risk. Perinatal infections Most of the perinatal pathogens (Table 26.3) arise from the birth canal or blood. Some bacteria silently colonise the maternal genital and gastrointestinal tracts until ascending infection produces severe and disseminated disease in the baby. Such infections are more common when there has been premature rupture of membranes. Early-onset infection in the neonate (within the first week of life) usually presents as a severe septicaemia, whereas, late-onset disease often presents as meningitis. Other organisms are genital pathogens that may be acquired during delivery and generally cause localised rather then systemic infections. Eye infection in the newborn is known as ophthalmic neonatorum. Postnatal infections Infection acquired after birth may be associated with cross-infection from babies, their mothers and attendant staff in nurseries and neonatal intensive care units (Fig. 26.1). Staphylococcal infections are usually minor but may present as the 'scalded skin' syndrome. Gastroenteritis (bacterial or viral) can be life-threatening in low-birth-weight babies. Diagnosis and management of neonatal infections TORCH is an acronym for a screen for infections that are associated with neonatal disease. It stands for Toxoplasama, Rubella, Cytomegalovirus and Herpes simplex. It is a useful aide memoire but is by no means all-inclusive. Diagnosis of these infections is mainly serological, although the herpesviruses can be grown from infected sites. If confirmed then treatment (not available for rubella) should be given if symptomatic or, in the case of toxoplasma infections, even if asymptomatic to prevent long-term sequelae. Chlamydial infections are detected by i mmunofluorescence or ELISA and treated with topical antibiotics. With suspected covert bacterial infection, blood cultures and CSF must be cultured promptly together with swabs of superficial sites (e.g. umbilicus, ear and rectum). Urgent antibacterial treatment should then be started. Risk factors for group B streptococcal disease can be identified and pregnant women screened for carriage of the organism in the vagina and rectum. Antibiotic prophylaxis is given to at-risk mothers during labour and to the baby after birth. Some viruses, e.g. HIV, may be transmitted by breast-feeding, which should be avoided. Scrupulous attention to aseptic techniques and other infection control procedures is essential in the care of neonates. Puerperal infections (postnatal infections in the mother) Puerperal sepsis, caused by group A streptococci, is now uncommon since the introduction of hand washing by attendants and associated procedures. Other organisms associated with puerperal infections include anaerobes and coliforms that may be introduced during instrumentation, especially septic abortions. The risk of infection is also increased if products of conception are retained in the uterus. Blood cultures and carefully taken high vaginal swabs should be sent and empirical antibiotic treatment started. Staph. aureus may cause breast abscesses in the mother a week or so after birth. 6 3 Congenital infections Organism Clinical features Laboratory diagnosis Preventative strategy Rubella Microcephaly, cataracts, deafness, heart defects, hepatosplenomegaly Rubella IgM in cord blood Virus isolation (throat, urine) Vaccination in childhood Screening in pregnancy Cytomegalovirus Deafness, mental retardation CMV IgM in cord blood Virus isolation (throat, urine) No current vaccine Varicella-zoster Skin, CNS and musculoskeletal abnormalities I solation of virus from vesicles, VZV IgM or rise in IgG Anti-varicella-zoster immunoglobulin (for infections late in pregnancy) Herpes simplex Limb deformities, disseminated infection Virus isolation Caesarian section Prophylactic acyclovir Hepatitis B Hepatitis Surface antigen in cord blood / PCR Screening in pregnancy HBV immunoglobulin Vaccination of neonate HIV Failure to thrive, oral thrush, lymphadenopathy, hepatomegaly, childhood AIDS HIV PCR as maternal antibody persists for up to 18 months Screening in pregnancy Prophylactic antiretroviral therapy Treponema pallidum Lesions in skin, bones, teeth and cartilage Hepatosplenomegaly, lymphadenopathy T pallidum I gM in fetus Screening in pregnancy Treatment of mother (early pregnancy) Toxoplasma gondii Microcephaly, eye lesions, Hepatosplenomegaly, jaundice Toxoplasma IgM in cord blood Selected screening in pregnancy Avoidance of primary infection Treatment of infection in pregnancy Listeria monocytogenes Septicaemia, meningitis, granulomas Bacterial culture None Parvovirus Anaemia, ascites, hepatosplenomegaly (hydrops fetalis) Parvovirus IgM/PCR in cord blood None Effects of pregnancy on i nfection Perinatal infections More severe May reactivate Organism Clinical features Route of infection Urinary tract infections Cytomegalovirus (CMV) Group B haemolytic streptococci Meningitis, septicaemia Ascending or Candida vulvovaginitis Herpes simplex virus during delivery Esch. coli I nfluenza Epstein-Barr virus Listeria monocytogenes Chicken pox (pneumonia) Polyomavirus (BK, JC) Viral hepatitis N. gonorrhoeae Conjunctivitis During delivery Poliomyelitis Chlamydia trachomatis Conjunctivitis, pneumonia Papillomavirus Laryngeal warts Malaria Lists riosis Herpes simplex virus Skin lesions, Maternal blood Coccidioidomycosis disseminated infection at delivery Hepatitis B virus Generalised infection HIV FIG 26.7 Routes of fetal and neonatal infection [...]... cell count acute phase response (T plasma viscosity and C-reactive protein) I nfections of bone - osteomyelitis Infections may be classified as acute or chronic The most frequent sites of infection are the lower li mbs and the humerus In acute osteomyelitis, X-rays may not show an abnormality at presentation, but computerised tomography (CT) or white-cell scans can be helpful Systemic features are less... present Periosteal reaction, cysts or sequestra (dead bone within a cavity) may be seen on X-ray (Fig 27.2) Blood cultures should always be taken and may be positive in about 50 % of cases Surgical material should be obtained for urgent microscopy and culture, particularly in chronic infections to guide long-term therapy Treatment may require both surgical drainage (which is usually essential in chronic... nvestigation and management X-rays show distension of the joint capsule and soft-tissue swelling - destructive changes are only seen in cases which present late These findings are not diagnostic of infection, and inflammatory conditions (e.g rheumatoid arthritis and gout) need to be considered Blood cultures should be taken and joint fluid aspirated In bacterial infections about 50 % of aspirates show bacteria... (see Table 27.1), but empirical therapy should include an anti-staphylococcal agent Acute infections generally require 3-6 weeks therapy, but in chronic cases treatment should continue for several months with close monitoring of response The parenteral route should be used for at least the first week and preferably longer Infections of joints - arthritis Septic arthritis (Table 27.1) Most bacterial joint...M E D I C A L MICROBIOLOGY I nfections of bone, joints and muscle Infections of bone and joint may arise from a number of sources (Fig 27.1) Predisposing factors include: • age - infections are commoner in neonates and the elderly • pre-existing local pathology, e.g trauma, tumours, sickle cell disease distant sites of infection,... spread and lead to septic arthritis with joint effusions, most commonly in the knee or hip Chronic infections may develop, particularly with mycobacteria or fungi 64 Reactive arthritis (Table 27.2) The sterile arthritis caused by an immune response to an infection is termed post-infectious or reactive arthritis In many cases this follows infection with enteric pathogens and is associated with the HLA... Acute bacterial arthritis requires 2-3 weeks antibiotic treatment, initially by the i.v route Open surgical drainage may also be necessary Prosthetic joint infections have an incidence of < 1 % following hip or knee replacement but are very difficult to diagnose and treat Most infections are probably acquired at operation and often present months later Coagulase-negative staphylococci are common pathogens... muscle Acute bacterial cellulitis caused by Group A (3-haemolytic streptococci may involve underlying fascia and muscles Gangrene may follow trauma or infection with mixed organisms, including streptococci, anaerobes and coliforms Both potentially fatal infections require prompt antibiotic therapy and full surgical debridement Viral myositis produces self-limiting muscle pain and may be caused by coxsackieviruses, . features Normal Vagina <4 .5 - Lactobacilli Minimal discharge, variable colour Candidiasis Vagina <4 .5 - Budding yeasts/hyphae Yellowish-white discharge/plaques, pruritus Trichomoniasis Vagina > 4 .5 Malodour Motile. frothy foul-smelling yellow-green discharge, Bacterial vaginosis Vagina > 4 .5 Malodour Clue cells vaginal petechiae Foul-smelling grey-white discharge, pruritus, dyspareunia +++ Gram-negative. with hepatitis B makes it more severe; super-infection results in recurrence I ncubation period 6-8 weeks. Water-borne Leptospira interrogans Faecal-oral epidemics have been seen in India and